Gamma-aminobutyric acid   中文名称: γ-氨基丁酸

- In weaning piglets: intestinal GABAergic system (including GABA transporters SLC6A13 and GABA receptor subunits GABA_B2 and GABA_Aβ2). [1]
- In Drosophila: GABA synthetic enzyme Gad1; ionotropic GABA receptors Lcch3 and RdI; metabotropic GABA receptors GABA-B-R1, -2, -3. [2]

γ-氨基丁酸 (30 μM) 使皮质祖细胞（E16 细胞）去极化，在心室区 (VZ) 细胞中引起内向电流，并在 5 μM 的半最大响应浓度下抑制 DNA 合成 [3]。 γ-氨基丁酸（1–5 μM；18 小时）可增加皮质板 (cp) 细胞的运动性并抑制迁移，而 G 蛋白激活则参与趋化信号传导。 GAD 由 cp 神经元表达。由于 γ-氨基丁酸激活 GABA A 受体，生长受到限制，细胞周期停滞在 S 期 [5]。

在断奶仔猪中，日粮中添加GABA（20 mg/kg饲料，持续3周）显著提高了第三周的生长率，并降低了第二周的饲料转化率。同时增加了肾脏器官指数。 [1]
- GABA补充抑制了回肠中IL-22、促炎细胞因子IL-1和IL-18以及Muc1的mRNA表达；促进了抗炎细胞因子IFN-γ、IL-4、IL-10以及TLR6和MyD88的表达。 [1]
- GABA显著降低了回肠中GABA转运体SLC6A13以及GABA受体亚基GABA_B2和GABA_Aβ2的mRNA表达。 [1]
- GABA增加了回肠黏膜中多种氨基酸的水平（如丙氨酸、苯丙氨酸、色氨酸、脯氨酸、丝氨酸、苏氨酸、胱氨酸、酪氨酸、组氨酸、鸟氨酸、肌肽），但降低了血清中多种氨基酸的水平（组氨酸、丝氨酸、精氨酸、丙氨酸、脯氨酸、胱氨酸、赖氨酸、甲硫氨酸、异亮氨酸、亮氨酸、苯丙氨酸）。 [1]
- GABA补充调节了肠道菌群：降低了厚壁菌门（门水平）、梭菌纲（纲水平）和狭义梭菌属（属水平）的相对丰度；增加了变形菌门、拟杆菌门、蓝细菌门、梭杆菌门、放线菌门等。同时增加了群落丰富度（observed species、Chao1、ACE）和多样性（Shannon、Simpson、PD whole tree）。 [1]
- 在果蝇中，GABA由表达Gad1的细胞产生，这些细胞在脑中形成特定细胞簇。触角叶中，局部神经元（LN1和LN2L）和mACT投射神经元释放GABA。GABA受体（Lcch3、RdI、GABA-B-R2）在大多数触角叶神经元（包括投射神经元和局部神经元）中广泛表达。 [2]

---

γ-氨基丁酸（33.95、102.25、306.75 mg/kg；口服；单剂量）可以改善小鼠的睡眠能力[6]。 ？在暴露于邻苯二甲酸二(2-乙基己基)酯的大鼠 (DEHP) 中，γ-氨基丁酸（1、2、4? mg/kg/d；口服；30 天）可减少焦虑、改善食物消耗并修复与暴露相关的损伤[7]。

细胞迁移测定[4]
细胞类型：皮质板 (cp) 神经元
测试浓度： 1-5 μM
孵育时间： 18 小时
实验结果： 通过 G 蛋白激活促进运动，并通过 GABAA 受体介导的去极化诱导迁移阻断引诱剂。

- Piglet study: Sixteen healthy weaned piglets (21 days old, Duroc × Landrace × Landrace, average body weight 6.43 kg) were randomly assigned to two groups (n=8 per group). The control group received a basal corn- and soybean meal-based diet; the GABA group received the same diet supplemented with 20 mg/kg GABA. The experiment lasted 3 weeks. Piglets were housed individually at 25±2°C with free access to feed and water. Body weight and feed intake were monitored weekly. After 3 weeks, piglets were sacrificed, and blood, ileum, ileal mucosa, and luminal contents were collected. [1]
- Drosophila study: Adult female flies (5–10 days old) were used. In situ mRNA hybridization was performed on dissected brains using DIG-labeled probes against Gad1, Lcch3, RdI, GABA-B-R1, -R2, -R3. Fluorescent in situ hybridization was combined with GAL4-driven GFP expression to identify cell types. Antibody labeling (anti-GFP, anti-CD8, nc82) and confocal microscopy were used. [2]

---

Animal/Disease Models: Pathogen-free (SPF) Bagg albino (Balb/c) mice (18–20 g, 8 weeks old) [6]
Doses: 33.95, 102.25, 306.75 mg/kg single dose; administered at 20 mL/kg; Measured results in hrs (hrs (hours)): more effectively extend sleep time, increase sleep rate, and shorten sleep latency.

---

Animal/Disease Models: SD (SD (Sprague-Dawley)) rats induced by DEHP (500 mg/kg) [7]
Doses: 1, 2, 4 mg/kg
Route of Administration: po (oral gavage); combined administration; 30 days
Experimental Results: Treated with DEHP Levels of nitric oxide and nitric oxide synthase are diminished in rats.

Gamma-aminobutyric acid (GABA) is rapidly absorbed after oral administration, with peak plasma levels reached within approximately 60 minutes, followed by rapid clearance and undetectable concentrations within 24 hours; exogenous GABA exhibits poor penetration across the blood–brain barrier and is primarily metabolized by GABA transaminase (GABA‑T) in peripheral tissues. In terms of toxicity, GABA demonstrates very low acute toxicity with an oral LD₅₀ of around 12,680 mg/kg in mice, and at physiological or moderate supplemental doses, it is generally safe, while excessive intake may elicit mild adverse effects including drowsiness, dizziness, transient hypotension, gastrointestinal discomfort, and at high doses, potential central nervous system depression, muscle weakness, or respiratory suppression; no significant carcinogenicity has been identified, and adverse reactions are dose‑dependent and mostly reversible upon discontinuation.

Chronically high levels of GABA are associated with at least 5 inborn errors of metabolism including: D-2-Hydroxyglutaric Aciduria, 4-Hydroxybutyric Aciduria/Succinic Semialdehyde Dehydrogenase Deficiency, GABA-Transaminase Deficiency, Homocarnosinosis and Succinic semialdehyde dehydrogenase deficiency.

---

119 mouse LD50 intraperitoneal 4950 mg/kg BEHAVIORAL: GENERAL ANESTHETIC; BEHAVIORAL: ALTERED SLEEP TIME (INCLUDING CHANGE IN RIGHTING REFLEX); LUNGS, THORAX, OR RESPIRATION: OTHER CHANGES Archivum Immunologiae et Therapiae Experimentalis., 13(70), 1965 [PMID:14291430]
119 rat LDLo intracrebral 18 mg/kg Biochemical Pharmacology., 14(1901), 1965 [PMID:5880545]
119 cat LD50 intravenous 5 gm/kg Russian Pharmacology and Toxicology, 47(205), 1984
119 mouse LD50 oral 12680 mg/kg Yakugaku Zasshi. Journal of Pharmacy., 85(463), 1965 [PMID:5318985]
119 rat LD50 intravenous >5 gm/kg United States Patent Document., #3380887

[1]. Effects of dietary gamma-aminobutyric acid supplementation on the intestinal functions in weaning piglets. Food Funct. 2019 Jan 22;10(1):366-378.

[2]. Gamma-aminobutyric acid (GABA)-mediated neural connections in the Drosophila antennal lobe. J Comp Neurol. 2009 May 1;514(1):74-91.

- GABA is synthesized from glutamate by glutamic acid decarboxylase (GAD). In the Drosophila brain, Gad1 is expressed in specific cell clusters, while Gad2 (black gene) is expressed mainly in the lamina. [2]
- In the piglet intestine, GABAergic system components (GABA transporters and GABA receptors) are expressed, and dietary GABA can modulate their expression. GABA may improve weaning stress by regulating intestinal immunity, amino acid profiles, and gut microbiota. [1]

---

Gamma-aminobutyric acid is a gamma-amino acid that is butanoic acid with the amino substituent located at C-4. It has a role as a signalling molecule, a human metabolite, a Saccharomyces cerevisiae metabolite and a neurotransmitter. It is a gamma-amino acid and a monocarboxylic acid. It is functionally related to a butyric acid. It is a conjugate acid of a gamma-aminobutyrate. It is a tautomer of a gamma-aminobutyric acid zwitterion.
The most common inhibitory neurotransmitter in the central nervous system.
gamma-Aminobutyric acid is a metabolite found in or produced by Escherichia coli (strain K12, MG1655).
4-Aminobutanoate has been reported in Angelica gigas, Microchloropsis, and other organisms with data available.
Gamma-Aminobutyric Acid is a naturally occurring neurotransmitter with central nervous system (CNS) inhibitory activity. Gamma-aminobutyric acid (GABA), converted from the principal excitatory neurotransmitter glutamate in the brain, plays a role in regulating neuronal excitability by binding to its receptors, GABA-A and GABA-B, and thereby causing ion channel opening, hyperpolarization and eventually inhibition of neurotransmission.
Gamma-aminobutyric acid (GABA) is an inhibitory neurotransmitter found in the nervous systems of widely divergent species. It is the chief inhibitory neurotransmitter in the vertebrate central nervous system. In vertebrates, GABA acts at inhibitory synapses in the brain. GABA acts by binding to specific transmembrane receptors in the plasma membrane of both pre- and postsynaptic neurons. This binding causes the opening of ion channels to allow either the flow of negatively-charged chloride ions into the cell or positively-charged potassium ions out of the cell. This will typically result in a negative change in the transmembrane potential, usually causing hyperpolarization. Three general classes of GABA receptor are known. These include GABAA and GABAC ionotropic receptors, which are ion channels themselves, and GABAB metabotropic receptors, which are G protein-coupled receptors that open ion channels via intermediaries (G proteins). Neurons that produce GABA as their output are called GABAergic neurons, and have chiefly inhibitory action at receptors in the vertebrate. Medium Spiny Cells are a typical example of inhibitory CNS GABAergic cells. GABA exhibits excitatory actions in insects, mediating muscle activation at synapses between nerves and muscle cells and also the stimulation of certain glands. GABA has also been shown to have excitatory roles in the vertebrate, most notably in the developing cortex. Organisms synthesize GABA from glutamate using the enzyme L-glutamic acid decarboxylase and pyridoxal phosphate as a cofactor. It is worth noting that this involves converting the principal excitatory neurotransmitter (glutamate) into the principal inhibitory one (GABA). Drugs that act as agonists of GABA receptors (known as GABA analogues or GABAergic drugs) or increase the available amount of GABA typically have relaxing, anti-anxiety and anti-convulsive effects. Doses of GABA 1 to 3 g orally also have been used effectively to raise the IQ of mentally retarded persons. GABA is found to be deficient in cerebrospinal fluid and brain in many studies of experimental and human epilepsy. Benzodiazepines (such as Valium) are useful in status epilepticus because they act on GABA receptors. GABA increases in the brain after administration of many seizure medications. Hence, GABA is clearly an antiepileptic nutrient. Inhibitors of GAM metabolism can also produce convulsions. Spasticity and involuntary movement syndromes, e.g., Parkinson's, Friedreich's ataxia, tardive dyskinesia, and Huntington's chorea are all marked by low GABA when amino acid levels are studied. Trials of 2 to 3 g of GABA given orally have been effective in various epilepsy and spasticity syndromes. Agents that elevate GABA also are useful in lowering hypertension. Three grams orally have been effective in control of blood pressure. GABA is decreased in various encephalopathies. GABA can reduce appetite and is decreased in hypoglycemics. GABA reduces blood sugar in diabetics. Chronic brain syndromes can also be marked by deficiency of GABA; GABA has many promising uses in therapy. Cerebrospinal fluid levels of GABA may be useful in diagnosing very serious diseases. Vitamin B6, manganese, taurine and lysine can increase both GABA synthesis and effects, while aspartic acid and glutamic acid probably inhibit GABA effects. The brain's principal inhibitory neurotransmitter, GABA, along with serotonin and norepinephrine, is one of several neurotransmitters that appear to be involved in the pathogenesis of anxiety and mood disorders. There are two principal subtypes of postsynaptic GABA receptor complexes, the GABA-A and GABA-B receptor complexes. Activation of the GABA-B receptor by GABA causes neuronal membrane hyperpolarization and a resultant inhibition of neurotransmitter release. In addition to binding sites for GABA, the GABA-A receptor has binding sites for benzodiazepines, barbiturates, and neurosteroids. GABA-A receptors are coupled to chloride ion channels; activation of the receptor induces increased inward chloride ion flux, resulting in membrane hyperpolarization and neuronal inhibition. After release into the synapse, free GABA that does not bind to either the GABA-A or GABA-B receptor complexes can be taken up by neurons and glial cells. Four different membrane transporter proteins, known as GAT-1, GAT-2, GAT-3, and BGT-1, which differ in their distribution in the CNS, are believed to mediate the uptake of synaptic GABA into neurons and glial cells. The GABA-A receptor subtype regulates neuronal excitability and rapid changes in fear arousal, such as anxiety, panic, and the acute stress response. Drugs that stimulate GABA-A receptors, such as the benzodiazepines and barbiturates, have anxiolytic and anti-seizure effects via GABA-A-mediated reduction of neuronal excitability, which effectively raises the seizure threshold. In support of the anticonvulsant and anxiolytic effects of the GABA-A receptor are findings that GABA-A antagonists produce convulsions in animals and the demonstration that there is decreased GABA-A receptor binding in a positron emission tomography (PET) study of patients with panic disorder. Low plasma GABA has been reported in some depressed patients and, in fact, may be a useful trait marker for mood disorders.
The most common inhibitory neurotransmitter in the central nervous system.
See also: ... View More ...

C4H9NO2

103.1198

103.063

56-12-2

53504-43-1;5959-35-3 (hydrochloride);6610-05-5 (mono-hydrochloride salt);70582-09-1 (calcium salt (2:1))

119

White to off-white solid powder

1.1±0.1 g/cm3

248.0±23.0 °C at 760 mmHg

195-204ºC

103.8±22.6 °C

0.0±1.0 mmHg at 25°C

1.465

-0.64

63.32

2

3

3

7

62.7

0

O([H])C(C([H])([H])C([H])([H])C([H])([H])N([H])[H])=O

BTCSSZJGUNDROE-UHFFFAOYSA-N

InChI=1S/C4H9NO2/c5-3-1-2-4(6)7/h1-3,5H2,(H,6,7)

4-aminobutanoic acid

DF468; gamma-aminobutyric acid; GABA; 56-12-2; Piperidic acid; Piperidinic acid; DF 468; Aminalon

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

注意： 本产品在运输和储存过程中需避光。

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

H2O : ~50 mg/mL (~484.87 mM)

配方 1 中的溶解度: 100 mg/mL (969.74 mM) in PBS (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液; 超声助溶。 (<60°C).

---

请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。